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<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">phkinetica</journal-id><journal-title-group><journal-title xml:lang="ru">Фармакокинетика и Фармакодинамика</journal-title><trans-title-group xml:lang="en"><trans-title>Pharmacokinetics and Pharmacodynamics</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2587-7836</issn><issn pub-type="epub">2686-8830</issn><publisher><publisher-name>ООО «Издательство ОКИ»</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.37489/2588-0519-2024-3-3-19</article-id><article-id custom-type="edn" pub-id-type="custom">EZRHZW</article-id><article-id custom-type="elpub" pub-id-type="custom">phkinetica-423</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>ОБЗОРЫ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>REVIEWS</subject></subj-group></article-categories><title-group><article-title>Сенесенс. Сердце. Сенотерапия</article-title><trans-title-group xml:lang="en"><trans-title>Senesens. Heart. Senotherapy</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-2832-4739</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Крыжановский</surname><given-names>С. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Kryzhanovskii</surname><given-names>S. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Крыжановский Сергей Александрович, д. м. н., зав. лабораторией фармакологии кровообращения</p><p>Москва</p></bio><bio xml:lang="en"><p>Sergey A. Kryzhanovskii, PhD, Dr. Sci. (Med.), Head of Laboratory of Circulation Pharmacology </p><p>Moscow</p></bio><email xlink:type="simple">kryzhanovskij_sa@academpharm.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-7407-7516</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Вититнова</surname><given-names>М. Б.</given-names></name><name name-style="western" xml:lang="en"><surname>Vititnova</surname><given-names>M. B.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Вититнова Марина Борисовна, к. б. н., в. н. с. лаборатории фармакологиикровообращения</p><p>Москва</p></bio><bio xml:lang="en"><p>Marina B. Vititnova, PhD, Cand. Sci. (Biology), Leading Researcher of Laboratory of Circulation Pharmacology </p><p>Moscow</p></bio><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБНУ «ФИЦ оригинальных и перспективных биомедицинских и фармацевтических технологий»</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Federal research center for innovator and emerging biomedical and pharmaceutical technologies</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2024</year></pub-date><pub-date pub-type="epub"><day>28</day><month>11</month><year>2024</year></pub-date><volume>0</volume><issue>3</issue><fpage>3</fpage><lpage>19</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Крыжановский С.А., Вититнова М.Б., 2024</copyright-statement><copyright-year>2024</copyright-year><copyright-holder xml:lang="ru">Крыжановский С.А., Вититнова М.Б.</copyright-holder><copyright-holder xml:lang="en">Kryzhanovskii S.A., Vititnova M.B.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://www.pharmacokinetica.ru/jour/article/view/423">https://www.pharmacokinetica.ru/jour/article/view/423</self-uri><abstract><p>Сенесенс — клеточное старение — особая форма гибели клетки, характеризующаяся необратимой утратой клеткой её пролиферационного потенциала и развитием устойчивости к апоптозу. В основе сенесенса лежит истирание (укорочение) теломер, происходящее при каждом последующем делении клетки, что, в конечном итоге, приводит к устойчивому повреждению ДНК и последующей активации программы клеточного старения. Сенесцентным клеткам присущ уникальный так называемый сенесенс-ассоциированный секреторный фенотип (SASP), т. е. способность стареющих клеток секретировать во внеклеточную среду большое количество патогенных факторов, действующих паракринно на неповреждённые клетки и переводящих их в состояние сенесенса. В обзоре литературы рассматриваются известные механизмы, ответственные за формирование различных типов сенесенса, описываются особенности сенесенс-обусловленного поражения сердца и приводится подробная характеристика биологически активных соединений и лекарственных средств, обладающих сенолитической (активаторы апоптоза) и/или сеностатической (ингибиторы SASP) активностью.</p></abstract><trans-abstract xml:lang="en"><p>Senescence — cellular aging — is a special form of cell death, characterized by the cell’s irreversible loss of its proliferation potential and the development of resistance to apoptosis. Senescence is based on the attrition (shortening) of telomeres that occurs with each subsequent cell division, which ultimately leads to sustained DNA damage and subsequent activation of the cellular aging program. Senescent cells have a unique so-called senescence-associated secretory phenotype (SASP), i.e. the ability of aging cells to secrete into the extracellular environment a large number of pathogenic factors that act paracrine on undamaged cells and transfer them to a state of senescence. The literature review examines the known mechanisms responsible for the formation of various types of senescence, describes the features of senescence-related cardiac damage, and provides a detailed description of biologically active compounds and drugs with senolytic (apoptosis activators) and/or senostatic (SASP inhibitors) activity.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>клеточная гибель</kwd><kwd>теломеры</kwd><kwd>сенесенс</kwd><kwd>сенесенс-ассоциированный секреторный фенотип</kwd><kwd>сенолитики</kwd><kwd>сеностатики</kwd></kwd-group><kwd-group xml:lang="en"><kwd>cell death</kwd><kwd>senesence telomeres</kwd><kwd>senesence-associated secretory phenotype</kwd><kwd>senolytics</kwd><kwd>senostatics</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Vogt CI Untersuchungen über die Entwicklungsgeschichte der Geburtshelferkröte (Alytes obstetricans). 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